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Journal of Veterinary Internal Medicine May 2021Movement disorders are a heterogeneous group of clinical syndromes in humans and animals characterized by involuntary movements without changes in consciousness. Canine...
Movement disorders are a heterogeneous group of clinical syndromes in humans and animals characterized by involuntary movements without changes in consciousness. Canine movement disorders broadly include tremors, peripheral nerve hyperexcitability disorders, paroxysmal dyskinesia, and dystonia. Of these, canine paroxysmal dyskinesias remain one of the more difficult to identify and characterize in dogs. Canine paroxysmal dyskinesias include an array of movement disorders in which there is a recurrent episode of abnormal, involuntary, movement. In this consensus statement, we recommend standard terminology for describing the various movement disorders with an emphasis on paroxysmal dyskinesia, as well as a preliminary classification and clinical approach to reporting cases. In the clinical approach to movement disorders, we recommend categorizing movements into hyperkinetic vs hypokinetic, paroxysmal vs persistent, exercise-induced vs not related to exercise, using a detailed description of movements using the recommended terminology presented here, differentiating movement disorders vs other differential diagnoses, and then finally, determining whether the paroxysmal dyskinesia is due to either inherited or acquired etiologies. This consensus statement represents a starting point for consistent reporting of clinical descriptions and terminology associated with canine movement disorders, with additional focus on paroxysmal dyskinesia. With consistent reporting and identification of additional genetic mutations responsible for these disorders, our understanding of the phenotype, genotype, and pathophysiology will continue to develop and inform further modification of these recommendations.
Topics: Animals; Chorea; Dog Diseases; Dogs; Dyskinesias; Mutation; Phenotype
PubMed: 33769611
DOI: 10.1111/jvim.16108 -
Arquivos de Neuro-psiquiatria Apr 2020
Topics: Antiparkinson Agents; Dyskinesia, Drug-Induced; Dyskinesias; Humans; Levodopa; Parkinson Disease
PubMed: 32321051
DOI: 10.1590/0004-282X20200023 -
Movement Disorders : Official Journal... Apr 2023Paroxysmal kinesigenic dyskinesia (PKD) is a movement disorder characterized by recurrent and transient episodes of involuntary movements, including dystonia, chorea,... (Review)
Review
Paroxysmal kinesigenic dyskinesia (PKD) is a movement disorder characterized by recurrent and transient episodes of involuntary movements, including dystonia, chorea, ballism, or a combination of these, which are typically triggered by sudden voluntary movement. Disturbance of the basal ganglia-thalamo-cortical circuit has long been considered the cause of involuntary movements. Impairment of the gating function of the basal ganglia can cause an aberrant output toward the thalamus, which in turn leads to excessive activation of the cerebral cortex. Structural and functional abnormalities in the basal ganglia, thalamus, and cortex and abnormal connections between these brain regions have been found in patients with PKD. Recent studies have highlighted the role of the cerebellum in PKD. Insufficient suppression from the cerebellar cortex to the deep cerebellar nuclei could lead to overexcitation of the thalamocortical pathway. Therefore, this literature review aims to provide a comprehensive overview of the current research progress to explore the neural circuits and pathogenesis of PKD and promote further understanding and outlook on the pathophysiological mechanism of movement disorders. © 2023 International Parkinson and Movement Disorder Society.
Topics: Humans; Dystonia; Movement Disorders; Chorea; Dyskinesias
PubMed: 36718795
DOI: 10.1002/mds.29326 -
The Western Journal of Medicine Nov 1990Tardive dyskinesia is a potentially irreversible syndrome of involuntary hyperkinetic movements that occur in predisposed persons receiving extended neuroleptic... (Review)
Review
Tardive dyskinesia is a potentially irreversible syndrome of involuntary hyperkinetic movements that occur in predisposed persons receiving extended neuroleptic (antipsychotic) drug therapy. It is usually characterized by choreoathetoid dyskinesias in the orofacial, limb, and truncal regions, but subtypes of this syndrome may include tardive dystonia and tardive akathisia. Although the mechanisms underlying the pathogenesis and pathophysiology of this disorder are unproven, altered dopaminergic functions will likely play a role in any explanation of it. Tardive dyskinesia develops in 20% of neuroleptic-treated patients, but high-risk groups such as the elderly have substantially higher rates. Risk factors include age, female sex, affective disorders, and probably those without psychotic diagnoses, including patients receiving drugs with antidopaminergic activity for nausea or gastrointestinal dysfunction for extended periods. Total drug exposure is positively correlated with tardive dyskinesia risk. Management strategies include a careful evaluation of both the psychiatric and neurologic states, a broad differential diagnosis, and adjustment of neuroleptic agents to the lowest effective dose that controls psychosis and minimizes motor side effects. No drug therapy is uniformly safe and effective for treating this disorder. A favorable long-term outcome of improvement or resolution correlates with younger age, early detection, lower drug exposure, and duration of follow-up.
Topics: Antipsychotic Agents; Child; Diagnosis, Differential; Dyskinesia, Drug-Induced; Humans; Movement Disorders; Prognosis; Risk Factors
PubMed: 1979705
DOI: No ID Found -
Zhurnal Nevrologii I Psikhiatrii Imeni... 2023Tardive dyskinesia (TD) is a delayed, often irreversible iatrogenic movement disorder caused by long-term use of that dopamine receptors blocking drugs. Prevention of TD...
Tardive dyskinesia (TD) is a delayed, often irreversible iatrogenic movement disorder caused by long-term use of that dopamine receptors blocking drugs. Prevention of TD is paramount, and clinicians should follow best practice recommendations for prescribing antipsychotics, as well as reduction the using of dopamine receptor blocking drugs for non-psychiatric prescriptions. Replacement of antipsychotics with lower affinity for D2 receptors drugs, addition of VMAT2 (tetrabenazine), botulinum therapy, amantadine may be effective. In detection and incurable cases, the possibility of neuromodulation of brain structures should be considered. Most methods for testing TD currently have an insufficient level of evidence, although they include recommendations from professional communities. There is a great need for new clinical trials.
Topics: Humans; Tardive Dyskinesia; Antipsychotic Agents; Tetrabenazine; Amantadine
PubMed: 37490662
DOI: 10.17116/jnevro202312307125 -
Neurobiology of Disease May 2022This review provides an overview of the synaptic dysfunctions of neuronal circuits and underlying neurochemical alterations observed in the hyperkinetic movement... (Review)
Review
This review provides an overview of the synaptic dysfunctions of neuronal circuits and underlying neurochemical alterations observed in the hyperkinetic movement disorders, dystonia and dyskinesia. These disorders exhibit similar changes in expression of synaptic plasticity and neuromodulation. This includes alterations in physical attributes of synapses, synaptic protein expression, and neurotransmitter systems, such as glutamate and gamma-aminobutyric acid (GABA), and neuromodulators, such as dopamine, acetylcholine, serotonin, adenosine, and endocannabinoids. A full understanding of the mechanisms and consequences of disruptions in synaptic function and plasticity will lend insight into the development of these disorders and new ways to combat maladaptive changes.
Topics: Antiparkinson Agents; Corpus Striatum; Dyskinesias; Dystonia; Dystonic Disorders; Humans; Levodopa
PubMed: 35139431
DOI: 10.1016/j.nbd.2022.105650 -
Journal of Neurochemistry Aug 2014Dopamine replacement therapy in Parkinson's disease is associated with several unwanted effects, of which dyskinesia is the most disabling. The development of new... (Review)
Review
Dopamine replacement therapy in Parkinson's disease is associated with several unwanted effects, of which dyskinesia is the most disabling. The development of new therapeutic interventions to reduce the impact of dyskinesia in Parkinson's disease is therefore a priority need. This review summarizes the key molecular mechanisms that underlie dyskinesia. The role of dopamine receptors and their associated signaling mechanisms including dopamine-cAMP-regulated neuronal phosphoprotein, extracellular signal-regulated kinase, mammalian target of rapamycin, mitogen and stress-activated kinase-1 and Histone H3 are summarized, along with an evaluation of the role of cannabinoid and nicotinic acetylcholine receptors. The role of synaptic plasticity and animal behavioral results on dyskinesia are also evaluated. The most recent therapeutic advances to treat Parkinson's disease are discussed, with emphasis on the possibilities and limitations of non-pharmacological interventions such as physical activity, deep brain stimulation, transcranial magnetic field stimulation and cell replacement therapy. The review suggests new prospects for the management of Parkinson's disease-associated motor symptoms, especially the development of dyskinesia. This review aims at summarizing the key molecular mechanisms underlying dyskinesia and the most recent therapeutic advances to treat Parkinson's disease with emphasis on non-pharmacological interventions such as physical activity, deep brain stimulation (DBS), transcranial magnetic field stimulation (TMS) and cell replacement therapy. These new interventions are discussed from both the experimental and clinical point of view, describing their current strength and limitations.
Topics: Animals; Cannabinoids; Cell Transplantation; Chromatin; Deep Brain Stimulation; Dopamine Agents; Dopamine and cAMP-Regulated Phosphoprotein 32; Dyskinesias; Histones; Humans; Levodopa; Motor Activity; Parkinson Disease; Phosphorylation; Psychomotor Performance; Receptors, Dopamine D1; Signal Transduction; Transcranial Magnetic Stimulation
PubMed: 24773031
DOI: 10.1111/jnc.12751 -
Ugeskrift For Laeger Jul 2021This is a case report of a patient, who was diagnosed with epilepsy (atypical infantile convulsions) at the age of one year and unspecific myopathy at the age of three...
This is a case report of a patient, who was diagnosed with epilepsy (atypical infantile convulsions) at the age of one year and unspecific myopathy at the age of three years. At the age of 25 years, the patient was referred to a neuromuscular clinic due to myopathy, but the diagnose was changed to atypical infantile convulsions with seizures in adulthood and paroxysmal choreoathetosis due to a pathogenic variant c.970G>A, p. (Gly324Arg) in the PRRT2 gene.
Topics: Adult; Dyskinesias; Epilepsy, Benign Neonatal; Humans; Infant; Membrane Proteins; Mutation; Nerve Tissue Proteins; Pedigree
PubMed: 34356019
DOI: No ID Found -
Expert Opinion on Drug Safety Dec 2019: Dyskinesia is a motor complication of Parkinson's disease (PD) characterized by clinical heterogeneity and complex pathogenesis and associated with long-term levodopa... (Review)
Review
: Dyskinesia is a motor complication of Parkinson's disease (PD) characterized by clinical heterogeneity and complex pathogenesis and associated with long-term levodopa therapy. Recent and controversial views on the management of PD patients have suggested that overall dyskinesia rates, and particularly troublesome dyskinesia, may be declining due to more conservative levodopa dosing regimens, widespread availability and early introduction of deep brain stimulation, and use of continuous drug delivery strategies. Nevertheless, anti-dyskinetic agents continue to be evaluated in clinical trials and recent efforts have focused on non-dopaminergic drugs.: In this review, the authors discuss the clinical phenomenology and current understanding of dyskinesia in PD with a focus on up-to-date therapeutic strategies to prevent and manage these drug-related involuntary movements.: The way dyskinesia in PD is currently managed should be changed and attention should be focused toward a more personalized medicine rather than a one-fits-all-approach. The correct identification of dyskinesia types and tailored treatments are crucial for a better management of these involuntary movements together with a holistic approach which considers additional influencing factors. The future for dyskinesia treatment is likely to be found in non-dopaminergic approaches, first set into motion by the introduction of amantadine.
Topics: Animals; Antiparkinson Agents; Deep Brain Stimulation; Drug Delivery Systems; Dyskinesia, Drug-Induced; Dyskinesias; Humans; Levodopa; Parkinson Disease
PubMed: 31619083
DOI: 10.1080/14740338.2019.1681966 -
Fortschritte Der Neurologie-Psychiatrie Apr 2019Tardive dyskinesias (TDs) are still common long-term sequelae of antipsychotic treatment. They are generally irreversible and associated with cognitive deficits, a... (Review)
Review
Tardive dyskinesias (TDs) are still common long-term sequelae of antipsychotic treatment. They are generally irreversible and associated with cognitive deficits, a decrease in quality of life and increased mortality. Furthermore, they potentially contribute to further stigmatization of the affected patients. However due to limited treatment options, antipsychotic drugs are still one of the cornerstones in treatment of most severe mental illnesses. Therefore, knowledge about risk factors and prevention of TDs is crucial. If TDs occur, the immediate optimization of the antipsychotic drug regimen is required. Targeted medical treatments such as VMAT - 2 inhibitors can be considered. The novel VMAT-2 inhibitors are not yet approved in Germany. Other drugs that are currently used to treat TDs include clonazepam and gingko biloba. This review summarizes the current evidence of treatment options of TDs and seeks to formulate clinical recommendations for the prevention and management of TDs.
Topics: Antipsychotic Agents; Dyskinesia, Drug-Induced; Germany; Humans; Quality of Life; Tardive Dyskinesia
PubMed: 29996156
DOI: 10.1055/a-0624-9368